UP-REGULATION OF TH-2 CYTOKINE RECEPTORS IN ATOPY-ASSOCIATED AND NONATOPY-ASSOCIATED CHRONIC SINUSITIS

Citation
Tc. Kotsimbos et al., UP-REGULATION OF TH-2 CYTOKINE RECEPTORS IN ATOPY-ASSOCIATED AND NONATOPY-ASSOCIATED CHRONIC SINUSITIS, Journal of otolaryngology, 25(5), 1996, pp. 317-321
Citations number
30
Categorie Soggetti
Otorhinolaryngology
Journal title
ISSN journal
03816605
Volume
25
Issue
5
Year of publication
1996
Pages
317 - 321
Database
ISI
SICI code
0381-6605(1996)25:5<317:UOTCRI>2.0.ZU;2-H
Abstract
Objective: This study was conducted to investigate the expression of a lpha IL5 and alpha GM-CSF receptors (alpha IL5r and alpha GM-CSFr) mRN A in the paranasal sinus mucosa of atopic and nonatopic subjects with chronic sinusitis compared to controls. Design: This was a prospective study of patients presenting with the diagnosis of chronic sinusitis of at least 6 months' duration. Method: Fourteen patients with stable chronic sinusitis (7 atopic, 7 nonatopic) and 7 controls were included , from whom sinus mucosal biopsies were obtained and examined for memb rane-bound alpha IL5r and alpha GM-CSFr mRNA using in situ hybridizati on. Results: There was a significant difference in the number of cells expressing alpha IL5r mRNA per high-power field in both atopic and no natopic subjects compared to controls, and in the number of cells expr essing alpha CM-CSFr mRNA in both atopic and nonatopic subjects compar ed with controls. The number of alpha IL5r mRNA-positive cells was sig nificantly greater in the atopic versus nonatopic groups, whereas alph a GM-CSFr mRNA-positive cells were greater in number in the nonatopic versus atopic groups. Conclusion: Both alpha IL5r and alpha GM-CSFr ar e upregulated in chronic sinusitis, suggesting that increases in both Th-2 cytokines and their receptors may be important in the pathology o f the disease. Furthermore, the predominant associations of alpha IL5r with atopic chronic sinusitis and alpha GM-CSFr with nonatopic chroni c sinusitis suggest that the chronic inflammation in this condition ma y arise from differential activation of distinct cytokine pathways dep ending on whether or not there is associated atopy.